One of the problems after a heart attack is the damage caused to heart tissue when blood flow is restored suddenly after a prolonged period without oxygen.

Blood flowing back into the tissues triggers production of harmful molecules, called free radicals, which are generated inside mitochondria - the powerhouses of the cell.

The new drug works by temporarily "switching off" the mitochondria for a few minutes to prevent a build-up of free radicals.

In the study, researchers tested the compound in a mouse model of heart attack.

It could potentially treat people immediately after a heart attack when blood flow to the heart is restored as part of routine treatmentShannon Amoils, British Heart Foundation

There were marked reductions in the total area of damaged heart tissue in mice given the drug compared with controls.

The researchers now hope to test their new compound in early human trials.

"MitoSNO effectively flicks a switch in the mitochondria, slowing down reactivation during those critical first minutes when blood flow returns and protecting the heart tissue from further damage," said Dr Mike Murphy from the Medical Research Council Mitochondrial Biology Unit, who led the study.

"We think a similar process happens in other situations where tissue is starved of oxygen for a prolonged period, for example after a stroke or during surgery where major arteries are clamped to prevent blood loss.

"We are hopeful that if human trials of MitoSNO are successful it could eventually be used in many other areas of medicine."

Commenting on the study, the British Heart Foundation, which part-funded the research, said the drug appeared promising.

"It could potentially treat people immediately after a heart attack when blood flow to the heart is restored as part of routine treatment," said research adviser Shannon Amoils.

"This could mean fewer heart attack survivors go on to live with the burden of heart failure, which for many is a debilitating and distressing condition."